For a solid tumor to grow to a certain size or above, angiogenesis is essential for ensuring sufficient supply of nutrition and oxygen to cancer cell (see, for example, New England Journal of Medicine, 1971, vol. 285, No. 21, pp. 1182-1186). One of the important factors causing angiogenesis toward tumor, a vascular endothelial growth factor (VEGF) is known. VEGF is bound to a vascular endothelial growth factor receptor (VEGFR) expressed on vascular endothelial cells and transmits signal for cell growth (see, for example, Endocrine Reviews, 1997, vol. 18, No. 1, pp. 4-25). Accordingly, inhibition of the VEGF-VEGFR signal transduction system is considered to enable suppression of angiogenesis and tumor growth (see, for example, Drug Discovery Today, 2001, vol. 6, No. 19, pp. 1005-1024). Moreover, since tumor blood vessels are involved in cancer hematogenous metastasis, inhibition of angiogenesis is considered to be effective for suppression of cancer metastasis.
As compounds inhibiting receptor-type tyrosine kinase including VEGFR, phthalazine derivatives (see, for example, WO 98/35958), pyrrole-substituted 2-indolinone derivatives see, for example, WO 01/60814), quinazoline derivatives (see, for example, WO 01/32651), ω-carboxyaryl-substituted diphenylurea derivatives (see, for example, WO 00/42012), quinoline derivatives and quinazoline derivatives (see, for example, WO 00/43366), nitrogen-containing aromatic ring derivatives (see, for example, WO 02/32872) and the like are known.